Arterial and venous vascular networks express different molecular markers and have different functions and branching architecture. Both arterial-venous identity specification and vascular branching during early embryogenesis are modulated by haemodynamic factors, but what is the nature of these factors? On p. 2187, Ferdinand le Noble and co-workers provide new insights into this question. They report that, in the chicken embryo yolk sac (vitelline) vasculature in vivo, a unique parameter related to the pulsatility of blood flow is significantly higher in arteries than in veins. They show that loss of this pulsatility reduces arterial marker expression in arterial cells both in vitro and in vivo. Then, by ligating vitelline arteries, they show that flow-driven collateral arterial network formation (arteriogenesis) is associated with increased arterial expression of Gja (connexin 40). Finally, they report that genetic ablation of Gja5 function in mice reduces arteriogenesis in two arterial occlusion models. Together, these results suggest that pulsatile flow and Gja5 expression modulate arterial identity and remodelling during flow-driven arteriogenesis.